bubble_chart Overview

Normal brain tissue has a strong ability to resist bacterial infections. Even in cases of open craniocerebral injury, as long as timely and thorough debridement is performed, the chance of developing a brain abscess is relatively low, accounting for only 5% of all brain abscess patients. The incidence of brain abscess in wartime firearm penetrating injuries is approximately 9%. Post-traumatic brain abscesses are often associated with retained bone fragments or foreign bodies. In firearm penetrating injuries, contaminated shrapnel remnants are more likely to cause infections compared to high-velocity bullets, as the latter generate high temperatures from friction during flight, achieving a sterilizing effect. Additionally, penetrating injuries entering the cranial cavity through the maxillofacial region, paranasal sinuses, or temporal/auricular regions and mastoid air cells significantly increase the likelihood of infection, especially if the patient has pre-existing paranasal sinus inflammation.

bubble_chart Pathogenesis

The onset time of traumatic brain abscess varies greatly, ranging from several weeks to many years after the injury, even up to several decades. The most common pathogenic bacteria are Staphylococcus aureus, followed by hemolytic streptococci and anaerobic streptococci, with occasional infections by Clostridium perfringens. Traumatic brain abscesses are mostly solitary but can be multilocular, and the thickness of the abscess wall varies with time. In the early stages of infection, around 2 weeks, it is in the stage of suppurative encephalitis and meningitis. At this time, brain tissue undergoes necrosis and softening, with marked inflammatory cell infiltration, congestion, and edema, and no abscess wall has formed yet. By about 3 weeks, the abscess forms, surrounded by granulation tissue, fibrous tissue, proliferation of reticuloendothelial cells and glial cells, forming a complete capsule. The thickness of the abscess wall is proportional to time, with a wall thickness of about 1mm at one month. In chronic abscesses that have persisted for a long time, the wall thickness may exceed the diameter of the abscess cavity.

bubble_chart Clinical Manifestations

The early acute inflammatory response of traumatic brain abscess is often masked by the brain injury itself. Symptoms such as fever, headache, increased intracranial pressure, and localized neurological dysfunction can easily be confused with the effects of brain trauma, especially when the abscess is located in non-functional areas of the brain, such as the frontal pole or temporal tip—so-called "silent areas"—leading to frequent misdiagnosis. Once the abscess forms, its clinical manifestations resemble those of an intracranial space-occupying lesion. At this stage, there are no signs of intracranial infection, only symptoms of elevated intracranial pressure, such as headache, drowsiness, bradycardia, or occasional seizures, with no other distinctive features. If the abscess is located in a critical functional area of the brain, local neurological deficits may aid in localization.

bubble_chart Diagnosis

The diagnosis of traumatic brain abscess mostly relies on specific auxiliary examinations, because once the abscess becomes localized, the patient not only shows no signs of elevated body temperature, but cerebrospinal fluid tests often reveal no abnormalities, or only a slight increase in white blood cells, which cannot serve as a diagnostic basis. Skull X-ray plain films help determine the presence of bone fragments or retained foreign objects. For larger brain abscesses, cerebral angiography can reveal midline structural shifts, avascular areas with a "ball-holding" appearance in blood vessels, or the "staining" phenomenon of capillary walls in the abscess, all of which aid in confirming the diagnosis. CT scanning is undoubtedly the most accurate and rapid diagnostic method, as it can display the size and location of the abscess, the number of abscesses, the presence of septations or gas, and their relationship with surrounding critical structures. Additionally, contrast-enhanced scans can assess the thickness of the abscess wall, helping estimate the abscess's stage and guiding the selection of appropriate treatment methods. MRI offers unique advantages, not only in the abscess formation stage by displaying a characteristic low-signal band around the necrotic area on T₂

-weighted images, but also in the encephalitis stage by enabling early diagnosis based on changes in T₁ and T₂ relaxation times. Specifically, on T₁-weighted images, irregular slightly low-signal areas can be seen in the white matter, while on T₂-weighted images, these areas appear as markedly high signals, with the encephalitis center showing slightly lower signals and mass effects. If Gd-DTPA enhancement is used, irregular diffuse enhancement can be observed on T₂-weighted images, providing valuable references for clinical treatment.

bubble_chart Treatment Measures

The treatment of traumatic brain abscess follows the same principles as otogenic or hematogenic brain abscesses. In general, when the abscess has not yet fully formed and is still in the stage of suppurative encephalitis, non-surgical methods can be employed, such as administering high-dose potent antibacterial drugs. This approach is particularly effective for cases with multiple small lesions or deep-seated abscesses that are unsuitable for surgical removal, often yielding satisfactory results through conservative treatment. However, for brain abscesses caused by retained intracranial foreign bodies post-trauma, which serve as infection foci, it remains questionable whether the formation of abscesses can be entirely prevented even during the suppurative encephalitis stage. For abscesses with well-formed walls, surgical intervention should be performed promptly. Typically, for abscesses with a short course, thin walls, and located in functionally critical areas of the brain, puncture and drainage are often preferred. For abscesses with a long course, thick walls, located in non-functional areas, or containing foreign bodies, surgical excision is more appropriate.

1. **Puncture and Drainage**: Based on the localization of the abscess, a non-functional area near the lesion is selected. Under local anesthesia, a cranial burr hole or twist-drill hole is made, and a brain needle is used to puncture the abscess. A distinct "give" sensation is often felt upon entering the abscess cavity. The needle is then advanced an additional 1–1.5 cm to prevent dislodgement. A syringe is used to slowly aspirate the pus. After about two-thirds of the pus has been drained, an equal volume of antibacterial saline (5 ml per wash) is used to repeatedly irrigate the cavity until the fluid runs clear. The brain needle is then withdrawn, and a silicone rubber tube or catheter is inserted along the same trajectory and depth as the initial puncture. Since the cavity still contains irrigation fluid, the drainage tube can be carefully adjusted to the optimal position for drainage. The tube is then brought out through the scalp puncture site and secured. The burr hole incision is closed in layers as usual without additional drainage. Postoperatively, the abscess cavity is irrigated daily or every other day with gentamicin (40,000–80,000 units) and saline solution. Systemic antibiotic therapy is continued, and follow-up CT scans are performed periodically until the abscess cavity closes, at which point the tube can be removed.

2. **Abscess Excision**: The procedure is performed under general anesthesia. A bone flap craniotomy is performed over the affected area, and the dura is incised in a curved fashion, selecting a non-functional area near the lesion. If intracranial pressure is not significantly elevated, the abscess can be directly approached through a cortical incision, dissected along the abscess wall, and completely excised to avoid contamination from pus leakage. If intracranial pressure is high or the abscess is large, a syringe is first used to aspirate the pus, followed by injection of gentamicin (40,000–80,000 units). The puncture site is then sealed with bipolar coagulation, and the abscess is bluntly dissected and excised along the surrounding edematous tissue. The surgical cavity is repeatedly irrigated with gentamicin (1,500 units/ml) or bacitracin (500–1,000 units/ml) dissolved in saline. The wound is closed in layers without drainage. Postoperative antibiotic therapy is continued until body temperature normalizes and cerebrospinal fluid tests return negative for 1–2 weeks.